Most studies which have attempted to produce hypertension (HT) in animals by utilizing various psychological stressors have failed. Those studies which have been moderately successful have only produced "borderline" HT. Recent studies from our laboratory have succeeded in producing severe HT in rats with one hypertensive parent. The HT appears permanent and is associated wih cardiac pathology. The current research seeks to determine some of the physiological correlates of conflict-induced HT. Specifically, rats with one hypertensive parent will be made hypertensive using conflict procedures. In one study, half of the rats exposed to conflict will be deprived of renal nerves to determine what role intact neural input to the kidneys plays in triggering and/or sustaining HT induced by stress. In a second study, half of the conflict-exposed animals will be exercised (swimming) for two hours daily to determine if exercise training protects against the delecterious cardiovascular effects of conflict. In two additional studies, the roles of the baroreceptors and alpha and beta adrenergic influences in the development of conflict-induced HT will be investigated. In the former study, phenylephrine injections in conscious stressed and unstressed rats will be compared. Sinoaortic denervation and light microscopy study of cross sections of the carotid arteries will be utilized to determine the source of any observed change in baroreceptor function with stress. The latter study will examine acute arterial blood pressure reponses to conflict in hypertensive, borderline hypertensive and normotensive rats studied with intact, alpha blocked and beta blocked innervations. A final study will chart the relationship between duration of conflict and the reversibility or irreversibility of conflict-induced HT. Th simultaneous assessment of markers of renal function (plasma renin activity and aldosterone), adrenal medullary (epinephrine and norepinephrine) and adrenal cortical function (corticosterone) will further characterize the mechanisms involved in producing conflict-induced HT. Finally, light and electron microscopy studies will allow us to detail the pathophysiological correlates of conflict-induced HT. This proposal will involve the disciplines of psychology, physiology and pharmacology.